DESCRIPTION (adapted from application): [unreadable] [unreadable] The long-term objectives of this research include (1) develop a versatile low-burden personal aerosol exposure platform for pulmonary diseases to sample and sense sized and speciated aerosols and link them with selected biological markers of disease severity; (2) add parallel acute and chronic metrics for outcomes where both exposure types apply; (3) plan how to add parallel exposure assessment capabilities to the platform to eventually address known and potential inhalation co-factors, including ozone, ultrafines, volatile organic compounds (VOCs), and carbonyls, as well as the confounder, environmental tobacco smoke (ETS); and (4) develop procedures and components that enable deployment of the personal platform in large-scale exposure biology etiology studies, including the methods for the associated data capture and validation. Focus areas of this proposal include the following: Personal Exposure: (1) develop an extremely small and lightweight real-time aerosol sensor with adequate specificity and sensitivity to characterize sized, breathing zone aerosol for children; (2) modify the design of the current RTI MicroPEM(tm) personal exposure platform to include the new aerosol sensor via a universal sensor interface for acute exposures; (3) include integrated (chronic) collections for aerosol mass and endotoxin while retaining the low-burden design; (4) integrate the aerosol sensor into the platform and allow real-time mass and endotoxin concentration estimates; (5) include global positioning system (GPS), activity level, and wearing compliance sensors; and (6) incorporate parallel integrated collections to assess ozone exposure (as a co-factor) and ETS (as a confounder). Exposure Biology: (1) in a limited-scale effort, demonstrate how urinary LTE4 levels for a pilot cohort of asthmatic children or adults can be related to real-time and integrated aerosol mass and endotoxin personal exposure levels through exposure biology models; (2) for participants in the pilot cohort determined to be passively exposed to ETS, relate urinary cotinine levels to elevated ETS levels in the integrated collection; and (3) include ozone as a potential co-factor in the models. The prevalence of pulmonary diseases, and especially asthma, in the United States for adults and children, combined with the existing uncertainties in linkages between personal exposures to known stressors such as aerosols and the resultant biological exacerbations, fully supports this research. [unreadable] [unreadable] [unreadable]